Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1.

ABSTRACT: Neutrophils can be beneficial or deleterious during tuberculosis (TB). Based on the expression of MHC-II and programmed death ligand 1 (PD-L1), we distinguished two functionally and transcriptionally distinct neutrophil subsets in the lungs of mice infected with mycobacteria. Inflammatory [MHC-II^-, PD-L1^lo] neutrophils produced inflammasome-dependent IL-1β in the lungs in response to virulent mycobacteria and "accelerated" deleterious inflammation, which was highly exacerbated in IFN-γR^-/- mice. Regulatory [MHC-II⁺, PD-L1^hi] neutrophils "brake" inflammation by suppressing T-cell proliferation and IFN-γ production. Such beneficial regulation, which depends on PD-L1, is controlled by IFN-γR signaling in neutrophils. The hypervirulent HN8

SUBMITTER: Doz-Deblauwe E 

PROVIDER: S-EPMC11109925 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature